The structural alteration of gut microbiota in low-birth-weight mice undergoing accelerated postnatal growth.
The structural alteration of gut microbiota in low-birth-weight mice undergoing accelerated postnatal growth.
复制标题
出生后加速生长的低出生体重小鼠肠道微生物群的结构变化。
DOI:
10.1038/srep27780
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发表时间:
2016-06-09
影响因子:
4.6
通讯作者:
Shen J
中科院分区:
文献类型:
--
作者:
Wang J;Tang H;Wang X;Zhang X;Zhang C;Zhang M;Zhao Y;Zhao L;Shen J
The transient disruption of gut microbiota in infancy by antibiotics causes adult adiposity in mice. Accelerated postnatal growth (A) leads to a higher risk of adult metabolic syndrome in low birth-weight (LB) humans than in normal birth-weight (NB) individuals, but the underlying mechanism remains unclear. Here, we set up an experiment using LB + A mice, NB + A mice, and control mice with NB and normal postnatal growth. At 24 weeks of age (adulthood), while NB + A animals had a normal body fat content and glucose tolerance compared with controls, LB + A mice exhibited excessive adiposity and glucose intolerance. In infancy, more fecal bacteria implicated in obesity were increased in LB + A pups than in NB + A pups, including Desulfovibrionaceae, Enterorhabdus, and Barnesiella. One bacterium from the Lactobacillus genus, which has been implicated in prevention of adult adiposity, was enhanced only in NB + A pups. Besides, LB + A pups, but not NB + A pups, showed disrupted gut microbiota fermentation activity. After weaning, the fecal microbiota composition of LB + A mice, but not that of NB + A animals, became similar to that of controls by 24 weeks. In infancy, LB + A mice have a more dysbiotic gut microbiome compared to NB + A mice, which might increase their risk of adult metabolic syndrome.